Health and Fitness

Asiatic Acid: Overview, Structure, Properties, and Formulas

Asiatic acid can be described as a triterpenoid pentacyclic, which is substituted with Ursane by the carboxy-group at 28, and the hydroxy groups in positions 2 3, 23, and (the 3beta, 2alpha stereoisomer). The molecule is isolated from Symplocos Lancifolia and Valeria indica and displays anti-angiogenic properties. Asiatic acid functions as an angiogenesis modulating agent, as well as a metabolic metabolite. The monocarboxylic acid triol and pentacyclic triterpenoid. It comes from a hydride of Ursane.

What are Asiatic Acid and Action mechanisms?

Asiatic acid (AA) triterpene reduced viability and caused apoptosis in HepG2 human Hepatoma cells in a dose-dependent way. The AA compound also significantly increased levels of intracellular Ca(2+) levels, which were inhibited by dantrolene and TMB-8 intracellular Ca(2+) release inhibitors and not EGTA as the extracellular Ca(2+) treatment. Additionally, apoptosis caused by AA was significantly reduced of TMB-8 and dantrolene and dantrolene, suggesting the intracellular Ca(2+) release could play a crucial role in the apoptosis induced by AA.

Furthermore, AA profoundly increased protein levels of p53. This was affected by BAPTA/AM and the intracellular Ca(2+) for chelation and TMB-8 and the dantrolene. Treatment with A23187 is one of the Ca(2+) Ionophore, or Thapsigargin and Ca(2+)-ATPase inhibitor, by itself increased the nuclear accumulation of p53, suggesting that p53 growth depends on the intracellular Ca(2+) increase. You can buy chemicals online.

Additionally, survival of Hep3B cells that were p53-null was significantly greater than that of HepG2 wild-type cells after treatment with AA. In total, these findings suggest that AA caused apoptosis by increasing intracellular Ca(2+) and results in increased the expression of p53 in HepG2 cells. These findings further suggest that AA could be an effective treatment of human Hepatomas.

Chemical and physical properties

 

Property Name Property Value Reference
Molecular Weight 488.7 Computed by PubChem 2.1 (PubChem release 2021.05.07)
XLogP3-AA 5.7 Computed by XLogP3 3.0 (PubChem release 2021.05.07)
Hydrogen Bond Donor Count 4 Computed by Cactvs 3.4.8.18 (PubChem release 2021.05.07)
Hydrogen Bond Acceptor Count 5 Computed by Cactvs 3.4.8.18 (PubChem release 2021.05.07)
Rotatable Bond Count 2 Computed by Cactvs 3.4.8.18 (PubChem release 2021.05.07)
Exact Mass 488.35017463 Computed by PubChem 2.1 (PubChem release 2021.05.07)
Monoisotopic Mass 488.35017463 Computed by PubChem 2.1 (PubChem release 2021.05.07)
Topological Polar Surface Area 98 ² Computed by Cactvs 3.4.8.18 (PubChem release 2021.05.07)
Heavy Atom Count 35 Computed by PubChem
Formal Charge 0 Computed by PubChem
Complexity 930 Computed by Cactvs 3.4.8.18 (PubChem release 2021.05.07)
Isotope Atom Count 0 Computed by PubChem
Defined Atom Stereocenter Count 12 Computed by PubChem
Undefined Atom Stereocenter Count 0 Computed by PubChem
Defined Bond Stereocenter Count 0 Computed by PubChem
Undefined Bond Stereocenter Count 0 Computed by PubChem
Covalently-Bonded Unit Count 1 Computed by PubChem
Compound Is Canonicalized Yes Computed by PubChem (release 2021.05.07)

Uses

Titrated extracts of Centella Asiatica (TECA) are composed of three main components: asiaticoside (AS), Asiatic acid (AA), and the madecassic acids (MA).  Asiatic acid is a triterpene from Centella Asiatica (L.) Urban (Umbelliferae) is registered as a treatment for dementia and to enhance cognition by Hoechst Aktiengesellschaft.

Parkinson’s (PD) disease is an incurable neurodegenerative disease that is a common occurrence of 1-2 percent in over 50. Mitochondrial dysfunction is joint in PD patients, who lose 15-30% of functioning in the complex. Asiatic acid (AA) triterpenoid is an antioxidant and is utilized to treat depression. 

However, the effectiveness of AA against PD-like damages is not known. In the current study, we examined the protective effects on the protective effects of AA on H(2)O(2) as well as rotenone-induced cell damage and mitochondrial dysfunction within SH-SY5Y cells. The mitochondrial membrane potential (MMP) and the voltage-dependent anion channel (VDAC) expression level were observed either with or without AA pretreatment after cellular injury to investigate the possible mechanisms behind AA neuroprotection. The results revealed that pretreatment with AAA (0.01-100 NM) protected cells from poisoning caused by rotenone or H(2)O(2).

Furthermore, MMP dissipation occurred following the exposure to rotenone which can be prevented with AA treatment. In addition, the pre-administration of AA prevented the increase in VDAC levels and mRNA levels caused by the exposure of rotenone (100 Nm) and H(2)O(2) (300 muM). These results suggest that AA may protect neurons against damage to mitochondria and suggests that AA may be developed to be a treatment for PD treatment or prevention.

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